Cancer is a complex continuum of diseases caused by gene mutations that disrupt the mechanisms controlling normal cell proliferation and survival. Unfortunately, many genes can be involved, which explains why cancers are so diverse in clinical behaviour and response to treatment. This knowledge has led to the expectation that more effective treatments will come from characterizing the defective regulatory pathways in individual cancers and inhibiting key components of each of these pathways. In practical terms this means that more effective cancer treatments will involve many therapeutic targets and a further refined understanding of how these targets regulate both normal and cancer cell behaviour. In our previous work we have studied the function of an enzyme called FER in the hope that it might represent a potential novel therapeutic target in cancer. We genetically engineered mice which no longer produce functional FER and found that they are overtly healthy, suggesting that humans might also tolerate inhibition of FER without serious toxicity; an important consideration for any therapeutic target. When these FER-deficient mice were bred to a separate strain of transgenic mice which develop breast cancer, we observed a significant reduction in tumor development. This result suggests that FER might represent a novel therapeutic target in breast cancer, and potentially other cancers as well. In this research proposal we aim to validate the effect of blocking FER on breast tumor development and determine if it is specific to one type of breast cancer or might also apply to other subtypes. We also learned a great deal in the previous grant term about how FER contributes to regulating cellular behaviour. We propose to extend this analysis to further refine that understanding in order to more fully appreciate how FER inhibition might block tumor development or metastasis.